Evidence map›Paper›PMID 25946076›Full record

ReviewBiomolecules2015

The Role of Reactive Oxygen Species (ROS) in the Formation of Extracellular Traps (ETs) in Humans.

Walter Stoiber, Astrid Obermayer, Peter Steinbacher, Wolf-Dietrich Krautgartner

Open access · goldAbstract readReview
In one paragraph

Review in Biomolecules, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 139 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
139citing papers in PubMed, 2 pooled it
6.8field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

139 citing papers in PubMed, 2 syntheses or guidelines pooled it, 243 citations in OpenAlex.

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  20. Brain-Death in Rats Increases Neutrophil Extracellular Trap Formation in Donor Organs.Transplant international : official journal of the European Society for Organ Transplantation · 2025
    Article

79 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Walter StoiberBiomedical Ultrastructure Research Group, Department of Cell Biology, University of Salzburg, Hellbrunnerstrasse 34, Salzburg A-5020, Austria. walter.stoiber@sbg.ac.at.
Astrid ObermayerBiomedical Ultrastructure Research Group, Department of Cell Biology, University of Salzburg, Hellbrunnerstrasse 34, Salzburg A-5020, Austria. astrid.obermayer@sbg.ac.at.
Peter SteinbacherBiomedical Ultrastructure Research Group, Department of Cell Biology, University of Salzburg, Hellbrunnerstrasse 34, Salzburg A-5020, Austria. peter.steinbacher@sbg.ac.at.
Wolf-Dietrich KrautgartnerBiomedical Ultrastructure Research Group, Department of Cell Biology, University of Salzburg, Hellbrunnerstrasse 34, Salzburg A-5020, Austria. wolf.krautgartner@sbg.ac.at.
University of Salzburg · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Extracellular traps (ETs) are reticulate structures of extracellular DNA associated with antimicrobial molecules. Their formation by phagocytes (mainly by neutrophils: NETs) has been identified as an essential element of vertebrate innate immune defense. However, as ETs are also toxic to host cells and potent triggers of autoimmunity, their role between pathogen defense and human pathogenesis is ambiguous, and they contribute to a variety of acute and chronic inflammatory diseases. Since the discovery of ET formation (ETosis) a decade ago, evidence has accumulated that most reaction cascades leading to ET release involve ROS. An important new facet was added when it became apparent that ETosis might be directly linked to, or be a variant of, the autophagy cell death pathway. The present review analyzes the evidence to date on the interplay between ROS, autophagy and ETosis, and highlights and discusses several further aspects of the ROS-ET relationship that are incompletely understood. These aspects include the role of NADPH oxidase-derived ROS, the molecular requirements of NADPH oxidase-dependent ETosis, the roles of NADPH oxidase subtypes, extracellular ROS and of ROS from sources other than NADPH oxidase, and the present evidence for ROS-independent ETosis. We conclude that ROS interact with ETosis in a multidimensional manner, with influence on whether ETosis shows beneficial or detrimental effects.

Indexed as

AutophagyExtracellular TrapsHumansMAP Kinase Signaling SystemNADPH OxidasesNeutrophilsReactive Oxygen SpeciesNADPH OxidasesReactive Oxygen Species

Identifiers

PMID25946076
PMCPMC4496692
OpenAlexW1565772479

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.